Article
Biochemistry & Molecular Biology
So Mee Kwon, Seongki Min, Un-woo Jeoun, Min Seok Sim, Gu Hyun Jung, Sun Mi Hong, Byul A. Jee, Hyun Goo Woo, Changhan Lee, Gyesoon Yoon
Summary: Cellular senescence is a permanent growth arrest state that can lead to aging. Splicing perturbation can induce senescence, with Sp1 identified as a key regulator in the process. Changes in spliceosomal gene composition can serve as an early marker for senescence.
Article
Biochemistry & Molecular Biology
Kimiyoshi Yano, Ryou-U Takahashi, Bunsyo Shiotani, Junko Abe, Tomoki Shidooka, Yuki Sudo, Yusuke Yamamoto, Shisei Kan, Hiroki Sakagami, Hidetoshi Tahara
Summary: PRPF19 is identified as a critical regulator of cellular senescence in normal human fibroblasts by modulating MDM4 splicing and p53 activity, leading to induction of p53-dependent cellular senescence.
JOURNAL OF BIOLOGICAL CHEMISTRY
(2021)
Article
Cell Biology
Li-Bin Gao, Ya-Hong Wang, Zhi-Hua Liu, Yu Sun, Peng Cai, Qing Jing
Summary: The study demonstrated that the small molecule SR9009 effectively suppresses the senescence-associated secretory phenotype (SASP) by activating the NRF2 pathway, preventing cellular senescence. It also showed efficacy in inhibiting cellular aging and inflammation in mouse models.
Article
Reproductive Biology
Xiaohong Yao, Chaofan Wang, Longjie Sun, Lu Yan, Xuexue Chen, Zheng Lv, Xiaomei Xie, Shuang Tian, Wenbo Liu, Lei Li, Hua Zhang, Jiali Liu
Summary: In this study, it was discovered that BCAS2 protein regulates pre-mRNA splicing in granulosa cells, affecting their proliferation and survival. BCAS2 participates in the PRP19 complex to mediate alternative splicing of E2f3 and Flt3l mRNA, thereby inhibiting the cell cycle. These findings reveal the function of BCAS2 in granulosa cells.
JOURNAL OF OVARIAN RESEARCH
(2023)
Review
Cell Biology
Lihuan Guan, Karen C. Crasta, Andrea B. Maier
Summary: This review highlights the significance of cellular senescence markers in human peripheral blood cells, summarizes related experiments and detection methods, as well as studies on demographic and clinical characteristics.
AGEING RESEARCH REVIEWS
(2022)
Article
Cell Biology
Jian-Xiong Xu, Mao -Lin Tang, Zhi-Feng Lu, Yu Song, Ke-Lan Zhang, Run-Chao He, Xiang-Na Guo, Yun-Qi Yuan, Xiaoyan Dai, Xin Ma
Summary: YPEL2 is expressed in tissues and organs enriched in vascular networks and plays a role in promoting senescence in human umbilical vein endothelial cells (HUVECs). YPEL2 is upregulated in atherosclerotic plaques and its deficiency can decrease senescence-associated beta-galactosidase (SA-beta-gal) activity and cell viability while reducing THP-1 cell adhesion and downregulating ICAM1 and VCAM1 expression. YPEL2 promotes cellular senescence via the p53/p21 pathway and may serve as a therapeutic target in aging-associated diseases.
MECHANISMS OF AGEING AND DEVELOPMENT
(2023)
Article
Cell Biology
Yiyang Sun, Lingling Zhang, Zhuoqing Fang, Dingyu Liu, Min Shao, Yujie Liu, Bing Liao, Ying Jin
Summary: The PRPF8 gene is essential for the survival of human embryonic stem cells (hESCs). Knockdown of PRPF8 induces p53 accumulation and activates the p53 pathway, leading to apoptosis in hESCs. PRPF8 regulates alternative splicing of PIRH2 to maintain p53 pathway activity and hESC survival.
JOURNAL OF CELLULAR PHYSIOLOGY
(2023)
Review
Oncology
Weronika Wojtys, Magdalena Oron
Summary: The development of RNA sequencing methods enables us to study and understand the aberrant pre-mRNA splicing in tumors. Altered splicing patterns affect various aspects of cancer development and are influenced by driver oncogenes. In turn, aberrant splicing activates key oncogenes and oncogenic pathways. Cancer research aims to improve diagnosis and treatment, and targeting alternative splicing mechanisms in the context of driver oncogenes presents potential therapeutic opportunities.
Article
Cell Biology
Luning Wang, Xiaohong Zhang, Junxiu Sheng, Lei Chen, Lili Zhi, Yangfan Qi, Qianqian Zheng, Linlin Wang, Jinrui Zhang, Jinyao Zhao, Yang Wang, Shu-Xin Liu, Ming-Zhong Sun, Wenjing Zhang
Summary: Cellular senescence is a powerful mechanism for inhibiting the proliferation of cancer cells, and RNA-binding proteins (RBPs) play important roles in regulating senescence. This study discovered that the RBP RBM4 contributes to cellular senescence and its depletion induces senescence in various cell types, including cancer cells. Furthermore, the depletion of RBM4 inhibits cancer cell progression and is mediated by the regulation of SERPINE1 through miR-1244.
CELL DEATH & DISEASE
(2023)
Review
Oncology
Jin Wu, Guanting Lu, Xinjiang Wang
Summary: MDM4, originally named MDMX, is an oncogene that plays critical roles in promoting cancer cell growth and inhibiting apoptosis by blocking the p53 pathway. Different splicing isoforms of MDM4 show potential therapeutic value in cancer treatment, making them attractive targets for therapy.
AMERICAN JOURNAL OF CANCER RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Shihui Lai, Yan Wang, Ting Li, Yihong Dong, Yihao Lin, Liang Wang, Shangeng Weng, Xiang Zhang, Chengjie Lin
Summary: CELF2 downregulation is associated with poor prognosis in pancreatic cancer. Abnormal expression of CELF2 affects the stemness, apoptosis, and proliferation of pancreatic cancer cells. The study also reveals that CELF2-mediated CD44 alternative splicing plays a role in tumorigenesis by regulating the endoplasmic reticulum-associated degradation pathway.
CELL AND BIOSCIENCE
(2022)
Article
Cell Biology
Yu Chen, Jie Sun, Zhenyu Ju, Zhao-Qi Wang, Tangliang Li
Summary: This study reveals the essential role of the DNA double-strand repair molecule Nbs1 in embryonic HSC development and hematopoiesis. Nbs1 deficiency leads to persistent DNA breaks in embryonic HSCs, affecting their development and causing perinatal lethality in mice. Additionally, the discrepancies in response to DNA damages between Nbs1 null HSCs and hematopoietic progenitors may be mediated by different levels of p53 signaling.
CELL PROLIFERATION
(2021)
Review
Cell Biology
Mikolaj Ogrodnik
Summary: The field of cellular senescence research has expanded rapidly from in vitro studies of aging to animal and clinical research, focusing on the role of senescence markers in aging, disease, and anti-senescence interventions. The presence and role of these markers in cells prior to cell cycle arrest, particularly in replicative aging and in vivo conditions, are discussed. The article also explores disparities in quantifications of senescence markers in vivo and the applicational value of broadening the cellular senescence paradigm.
Article
Biochemistry & Molecular Biology
Atsuya Tsuru, Mikihiro Yoshie, Junya Kojima, Ryo Yonekawa, Mana Azumi, Kazuya Kusama, Hirotaka Nishi, Kazuhiro Tamura
Summary: PGRMC1 is involved in cellular senescence during decidualization through the regulation of FOXO1 expression.
Article
Biology
Su-Jeong Lee, Da-Yeon Lee, Jennifer F. O'Connell, Josephine M. Egan, Yoo Kim
Summary: This study examined the impact of black ginseng (BG) on cellular senescence and found that BG supplementation can delay cellular senescence, particularly reducing activation of the canonical senescence pathway in multiple metabolic organs. The findings suggest that BG may be a potential senolytic candidate for retarding the aging process.